Both protectants and executioners have been reported to be played by gap junction in cerebral ischemia.To clarify this dispution, we explored the effects of its specific inhibitor octanol in focal cerebral ischemia rats (occlusion for 30 min and 2 h respectively and then reperfusion for 24 h).The results showed that octanol significantly enlarged infarction damage from (5.5±1.96)% to (16.11±3.35)% after 30 min occlusion, whereas octanol decreased the damage from to (45.53 ±9.51)% to (12.69±5.29)% after 2 h occlusion.Consistent with these results, octanol markedly increased the number of TUNEL-positive neurons after 30min occlusion, while opposite effects for 2 h occlusion.Our results indicate that gap junction can protect ischemic injury afer short term occlusion and aggravateitafter long time occlusion.